title: [What the surgeon needs to know about basic new concepts of inflammation and their therapeutic consequences: sanitation of inflammation is not a passive but rather an active process regulated by lipid mediators].
abstract: The acute inflammatory response as a physiological programme that protects the organism against injurious pathogens is characterised by highly regulated actions of pro- and anti-inflammatory mediators. Intensive investigations during the last decades have led to the identification of these mediators and their complex interplay as well as the design and development of anti-inflammatory therapies. However, the resolution of acute inflammation has long been considered to be a passive process. In consequence, little was known about the mechanisms which guide acute inflammation either to complete resolution, repair of inflamed tissue and restoration of normal function or to a chronic inflammatory process characterised by persistent signs of inflammation, tissue damage and impaired function. Predominantly during the last decade the so-called specialised proresolving mediators (SPM) have been identified. These essential fatty acid-derived mediators - lipoxins, resolvins, protectins, and maresins - terminate the acute inflammatory responses and stimulate their complete resolution. SPM possess both anti-inflammatory and proresolving activities in that they inhibit pro-inflammatory cytokines, limit infiltration of neutrophils, enhance macrophage uptake, and finally stimulate their non-phlogistic activation and clearance of apoptotic neutrophils and microbial particles. It has been demonstrated in multiple animal models of human inflammatory diseases that, e.g., atherosclerosis, diabetes, and inflammatory bowel diseases are caused by a decreased synthesis and/or an impaired signal transduction of the proresolving mediators. Future studies are warranted to clarify whether these proresolving lipid mediators will participate in healing human inflammatory diseases and their complications.
authors.affiliation: Pathologische Biochemie am Inst. für klinische Chemie & Pathobiochemie, Universitätsklinikum Magdeburg A. ö. R., Deutschland. andreas.gardemann@med.ovgu.de
authors.forename: A
authors.initials: A
authors.lastname: Gardemann
authors.forename: F
authors.initials: F
authors.lastname: Meyer
authors.forename: R
authors.initials: R
authors.lastname: Braun-Dullaeus
mesh_terms: D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D015525:Fatty Acids, Omega-3 / Q000502:physiology* / Q000627:therapeutic use; D043371:Fatty Acids, Omega-6 / Q000502:physiology* / Q000627:therapeutic use; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery*; D012307:Risk Factors; D018746:Systemic Inflammatory Response Syndrome / Q000209:etiology / Q000503:physiopathology* / Q000601:surgery
chemical_list: D000893:Anti-Inflammatory Agents; D015525:Fatty Acids, Omega-3; D043371:Fatty Acids, Omega-6